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Pancreatic immunoreactive somatostatin release.

G S Patton, E Ipp, R E Dobbs

    Proceedings of the National Academy of Sciences of the United States of America
    |May 1, 1977
    PubMed
    Summary
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    Glucagon and arginine stimulate somatostatin release from pancreatic D-cells, suggesting a local feedback mechanism. Insulin does not promptly increase somatostatin release, potentially modulating glucagon

    Area of Science:

    • Endocrinology
    • Pancreatic Physiology
    • Cell Signaling

    Background:

    • Pancreatic D-cells produce somatostatin, strategically located near A- and B-cells.
    • The proximity suggests a role for somatostatin in regulating insulin and glucagon secretion.

    Purpose of the Study:

    • To investigate if insulin and glucagon stimulate immunoreactive somatostatin (IRS) release from D-cells.
    • To explore the effect of secretogogues on IRS release and potential feedback mechanisms.

    Main Methods:

    • Isolated dog pancreases were perfused with varying concentrations of glucagon, insulin, or arginine.
    • Immunoreactive somatostatin (IRS) release was measured during perfusion experiments.
    • Glucagon and insulin levels were monitored in response to arginine stimulation.

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    Main Results:

    • Glucagon perfusion significantly increased IRS release (71-128%) within 40-100 minutes.
    • Insulin perfusion did not cause a prompt increase in IRS release; a rise was observed only after 100 minutes.
    • Arginine perfusion rapidly elevated IRS release (71-465%) and sustained it, while glucagon and insulin peaked early.

    Conclusions:

    • High doses of glucagon and arginine stimulate IRS release, supporting a local A-cell to D-cell feedback circuit.
    • Insulin does not appear to promptly augment IRS release.
    • Somatostatin stimulated by local glucagon may inhibit B-cell responses to glucagon, influencing the insulin/glucagon secretion mixture.